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1.
Sheng Li Xue Bao ; 75(6): 946-952, 2023 Dec 25.
Artigo em Chinês | MEDLINE | ID: mdl-38151356

RESUMO

Our previous study has shown that p66Shc plays an important role in the process of myocardial regeneration in newborn mice, and p66Shc deficiency leads to weakened myocardial regeneration in newborn mice. This study aims to explore the role of p66Shc protein in myocardial injury repair after myocardial infarction in adult mice, in order to provide a new target for the treatment of myocardial injury after myocardial infarction. Mouse myocardial infarction models of adult wild-type (WT) and p66Shc knockout (KO) were constructed by anterior descending branch ligation. The survival rate and heart-to-body weight ratio of two models were compared and analyzed. Masson's staining was used to identify scar area of injured myocardial tissue, and myocyte area was determined by wheat germ agglutinin (WGA) staining. TUNEL staining was used to detect the cardiomyocyte apoptosis. The protein expression of brain natriuretic peptide (BNP), a common marker of myocardial hypertrophy, was detected by Western blotting. The results showed that there was no significant difference in survival rate, myocardial scar area, myocyte apoptosis, and heart weight to body weight ratio between the WT and p66ShcKO mice after myocardial infarction surgery. Whereas the protein expression level of BNP in the p66ShcKO mice was significantly down-regulated compared with that in the WT mice. These results suggest that, unlike in neonatal mice, the deletion of p66Shc has no significant effect on myocardial injury repair after myocardial infarction in adult mice.


Assuntos
Infarto do Miocárdio , Estresse Oxidativo , Animais , Camundongos , Peso Corporal , Cicatriz/metabolismo , Camundongos Knockout , Infarto do Miocárdio/genética , Proteínas Adaptadoras da Sinalização Shc/metabolismo , Proteína 1 de Transformação que Contém Domínio 2 de Homologia de Src/genética , Proteína 1 de Transformação que Contém Domínio 2 de Homologia de Src/metabolismo
2.
Plants (Basel) ; 12(18)2023 Sep 11.
Artigo em Inglês | MEDLINE | ID: mdl-37765395

RESUMO

The rational development and efficient utilization of saline soils can alleviate the problem of insufficient arable land faced by agricultural production in China. A prominent problem is improving soil salt and water conditions for promoting land resources' productivity in coastal areas. Biochar is widely used for soil improvement, as it has remarkable properties. A pot experiment was conducted to study the effects of two kinds of biochar (common biochar and acid-modified biochar) with three addition rates (2%, 4%, and 8%) on the growth, yield, photosynthetic characteristics, and quality of spinach. The results revealed that 2% and 4% common biochar increased the plant height, stem diameter, and leaf area index, effectively improving the yield of spinach and water productivity, while 8% common biochar was detrimental to the growth of spinach to some extent. Acid-modified biochar significantly benefited the growth and increased the water productivity of spinach, ensuring high yields, while also improved quality. Similarly, acid-modified biochar was less effective at high additions than at low-to-medium additions. The integrated biological response version 2 (IBRV2) values under acid-modified biochar treatments were all significantly higher than those under common biochar, but there is no significant difference among three treatments in the same biochar group, which suggested a pronounced amelioration in spinach growth within saline-alkali soil upon the incorporation of acid-modified biochar. Overall, applying acid-modified biochar at the rate of 4% exhibited enormous potential for increasing the yield and quality of spinach in saline soils.

3.
J Mol Cell Cardiol ; 177: 21-27, 2023 04.
Artigo em Inglês | MEDLINE | ID: mdl-36827872

RESUMO

The longevity protein p66Shc is essential for the senescence signaling that is involved in heart regeneration and remodeling. However, the exact role of p66Shc in heart regeneration is unknown. In this study, we found that p66Shc deficiency decreased neonatal mouse cardiomyocyte (CM) proliferation and impeded neonatal heart regeneration after apical resection injury. RNA sequencing and functional verification demonstrated that p66Shc regulated CM proliferation by activating ß-catenin signaling. These findings reveal the critical role of p66Shc in neonatal heart regeneration and provide new insights into senescence signaling in heart regeneration.


Assuntos
Transdução de Sinais , Animais , Camundongos , Fosforilação , Proteínas Adaptadoras da Sinalização Shc/genética , Proteínas Adaptadoras da Sinalização Shc/metabolismo , Proteína 1 de Transformação que Contém Domínio 2 de Homologia de Src/genética , Proteína 1 de Transformação que Contém Domínio 2 de Homologia de Src/metabolismo
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